Sudden death syndrome is, as the name would suggest, a devastating disease. It first emerged in Arkansas in 1971 and has since spread across the US and even into South America by the 1990’s, causing heavy fatalities. The fungus that causes it, Fusarium virguliforme, can be considered the root of one of the most deadly soil-borne diseases out there.
Fighting Sudden Death
If you haven’t guessed by now at this facetious tone, sudden death syndrome (or SDS) is not something that affects humans or even animals at all. It is a disease of soybeans, so don’t worry too much about those previously mentioned fatalities. But this reveal shouldn’t diminish the concern one has for the disease, since it is truly a horror for soybean growers and much money and effort has been put into stopping its spread.
One complicated aspect of fighting the fungus is that the symptoms of its infection often don’t show up until late in the soybean life cycle, such as during flowering. And, by then, it’s often far too late. Farmers also have to carefully distinguish SDS from other diseases, since it can appear similar to many other conditions, such as brown stem rot, stem canker, and charcoal rot.
Now, there are already SDS resistance genes naturally found in soybeans, several dozen of them in fact. Though, alone, they often do not have enough of an effect to properly fight off the fungus. Research is, of course, already under way to test things like overexpression of these resistance genes in order to enhance soybean survivability.
But scientists at Iowa State University wanted to take a different tactic. They decided to utilize a plant defense feature known as nonhost resistance, which relates to plant immune responses when exposed to a pathogen that isn’t evolved to target said plant. In such a case, the defenses truly activate once the pathogen fails to invade and infect the plant in question.
The first and one of the most well studied of these defenses is the pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) response. This, in addition to many other protein and molecular pathway triggers, is the primary mechanism by which plants defend themselves when facing a nonhost pathogen attack. Plants that are hosts for the pathogen in question lack the capability (or time, usually) to start this defense since the initial pathogen invasion is often successful.
PAMPs, which themselves are molecules that the pathogens exhibit usually on their surface and that are recognized by the plants for the threat they are a part of, are the main instigators and thus regulators of the rest of the immune system response in plants. Once a PAMP has been recorded by a plant’s immune system, multilayered resistance abilities are activated by the plant.
In response, the pathogen takes a secondary step by releasing effector molecules that attempt to disrupt the plant’s defense mechanisms, thus causing effector triggered susceptibility. If a plant cell is affected by the effector, then the pathogen has a chance to get into the cell itself.
The arms race continues however, with the plant as a whole activating genes for receptors that recognize the effector molecules and enacting effector triggered immunity. This normally takes the form of cell hypersensitivity, where any cells found to be susceptible to the effectors activate their programmed cell death systems, thus preventing their infection by killing themselves.
Finding The Right Gene
In studying nonhost resistance, Arabidopsis is commonly used as the chosen model organism due to the expansive knowledge on its genome and the wide variety of knockout mutants available for almost every gene. Previous studies had shown that a knockout of the PSS1 gene caused susceptibility to several species of fungi, including F. virguliforme.
The scientists ran a genetic mapping of the gene to locate its chromosomal region and also mapped out six other PSS1 variant genes for investigation. Once they had identified their target gene, they used Agrobacterium to transfer it into transgenic soybean lines.
As a test for best expression, they used three different promoters in different experimental groups to see which would cause the best resistance response. One was a promoter that responds and is induced during infection, another was a root specific promoter that only expresses the gene in root cells (since the fungi attacks the plants from the soil), and the third promoter was from the original Arabidopsis gene itself.
Nonhost To Host Defenses
The soybean line chosen is known for being moderately susceptible to the fungus and, thus, was picked to best measure the presumably improved immune response. All of the three transformed experimental groups saw significantly reduced infection rates as compared to wild-type. But the root specific promoter group saw the best response, though only a hair better than the Arabidopsis promoter group. Overall, all three groups saw an average of a 85% reduction in the spread of the pathogen in the roots after infection.
The study authors noted that since nearly all the soybeans grown worldwide are transgenic anyways, adding varieties with this resistance trait would not meaningfully affect the regulatory burden on commercialization. This makes this gene and resistance method a great option to combat F. virguliforme and sudden death syndrome. It also reveals that the use of nonhost resistance genes from other plants may be a good method to deal with specific pathogens in crops and other grown plant varietals.
Photo CCs: Soybeans Schoharie Crossing State Historical Site, Fort Hunter NY 2807 from Wikimedia Commons